Journal of Gerontological Nursing

CE Article 

Normal Pressure Hydrocephalus: Are You Missing the Signs?

Sandra L. Siedlecki, PhD, RN, CNS

Abstract

Although normal pressure hydrocephalus (NPH) is a potentially treatable neurological condition, many individuals with NPH will never receive treatment because the diagnosis is missed and the symptoms are attributed to other disorders. Left untreated, NPH causes significant physical and emotional suffering and eventually leads to premature death. It is imperative that patients with gait problems, slowness of thought or actions, or urinary incontinence be evaluated and screened for NPH. Geriatric nurses are in the best position to intervene by recognizing the signs of NPH and making early and appropriate referrals.

Abstract

Although normal pressure hydrocephalus (NPH) is a potentially treatable neurological condition, many individuals with NPH will never receive treatment because the diagnosis is missed and the symptoms are attributed to other disorders. Left untreated, NPH causes significant physical and emotional suffering and eventually leads to premature death. It is imperative that patients with gait problems, slowness of thought or actions, or urinary incontinence be evaluated and screened for NPH. Geriatric nurses are in the best position to intervene by recognizing the signs of NPH and making early and appropriate referrals.

Dr. Siedlecki is Senior Nurse Researcher, Cleveland Clinic, Cleveland, Ohio.

The author discloses that she has no significant financial interests in any product or class of products discussed directly or indirectly in this activity, including research support.

Address correspondence to Sandra L. Siedlecki, PhD, RN, CNS, Senior Nurse Researcher, Cleveland Clinic, 9500 Euclid Avenue P32, Cleveland, OH 44195; e-mail: siedles@ccf.org.

Normal pressure hydrocephalus (NPH) was first described in 1965 after Adams, Fisher, Hakim, Ojemann, and Sweet identified a common triad of mild impairments in 6 older patients diagnosed with an expanding hydrocephalus associated with normal cerebrospinal fluid (CSF) pressure. These mild impairments consisted of an unsteady gait, slowness of thought and action, and urinary incontinence.

Although previously thought to be a rare disorder, improved screening and education about NPH has contributed to increases in the annual number of cases diagnosed and successfully treated, suggesting NPH may not be as rare as originally thought. It is estimated that more than 750,000 Americans have NPH, but less than 20% receive an appropriate diagnosis and treatment (Garden State Neurology & Neuro-Oncology, 2006; National Council on Aging, 2004). Because symptoms of NPH mimic those of other neurological disorders frequently encountered in older patients, NPH is often misdiagnosed as Parkinson’s disease or Alzheimer’s disease. In fact, 5% to 10% of all patients diagnosed with dementia are believed to actually have NPH (Chicago Institute of Neurology and Neuroresearch, 2007; Cleveland Clinic, n.d.; Garden State Neurology & Neuro-Oncology, 2006). However, NPH, unlike Parkinson’s disease and Alzheimer’s disease, is a potentially reversible neurological condition. Therefore, it is imperative health care providers learn to recognize the symptoms of NPH so early and appropriate referrals to specialists for treatment can be made.

Neurological Anatomy Review

The central nervous system consists of the brain and spinal cord. The spinal cord conducts sensory and motor information and serves as a reflex center. The brain receives and processes input from the spinal cord and initiates appropriate and coordinated responses. Both the brain and spinal cord are protected by three layers (dura mater, arachnoid mater, and pia mater) of connective tissue called meninges (Waxman, 2003). Pia mater is closest to the brain and spinal cord; dura mater is closest to the skull; and arachnoid mater, filled with CSF, is located between the other two membranes. The subarachnoid space separates the arachnoid and pia mater (Waxman, 2003).

CSF cushions the brain and spinal cord. The total amount of CSF at any one time is usually 140 mL to 150 mL, with approximately 500 mL of CSF removed and produced daily. CSF circulates from the lateral ventricles of the brain through the foramen of Monro into the third ventricle and then through the cerebral aqueduct into the fourth ventricle, where it then passes into the central canal of the spinal cord and into sub-arachnoid spaces around the brain. The fluid flows around the superior sagittal sinus and is reabsorbed into the venous system through arachnoid villa, aided by a pressure gradient differential between the CSF and venous systems (Cleveland Clinic Health Information Center, 2004).

Etiology of NPH

The etiology of NPH is unclear, and although some cases can be attributed to known neurological injuries, most are idiopathic. Symptoms associated with NPH are thought to be due to ventricular dilation. Two conflicting theories have been proposed to explain the ventricular dilation found in patients with NPH (McGirt et al., 2005). The first theory attributes ventricular dilation to CSF malabsorption, which results in cerebral ischemia, stretching of periventricular white matter (a group of nerve fibers to the side of the two lateral ventricles that conduct nerve impulses quickly and are important for muscle movement [MedFriendly.com, n.d.]), increased transmittal pressure, asymptomatic fibrosing meningitis (Medi-Fax Health Information Center, 1999), or insufficiency of the cortical extracellular space for CSF transit by way of the arachnoid space. Support for this theory is based in part on the success of CSF diversion in reversing symptoms (Walchenbach, Geiger, Thomeer, & Vanneste, 2002).

The second theory suggests ventricular dilation is unrelated to CSF malabsorption and is instead secondary to periventricular microvascular disease that leads to encephalomalacia (softening of the brain caused by infarct) and dilation of the cerebral ventricles. This hypothesis is supported by the observed association between idiopathic NPH and hypertension, ischemic heart disease, diabetes, and reduced high-density lipoprotein cholesterol (Casmiro et al., 1989). However, evidence from recent studies suggests that ventricular dilation is most likely the result of impaired CSF reabsorption at the arachnoid granulations or impaired CSF conduction through the subarachnoid space (McGirt et al., 2005).

Arachnoid granulations are small extensions of arachnoid mater that protrude through the dura mater and into the venous sinuses of the brain, allowing CSF to exit the brain (Waxman, 2003). A communicating hydrocephalus (hydrocephalus not caused by an obstruction) is produced when arachnoid granulations fail to sufficiently remove CSF fluid. This could be the result of fibrosis or scarring that disrupts surfaces and interfaces, or it could be a long-term condition that begins in childhood as the result of immature arachnoid granulations. When CSF removal is insufficient, a pressure gradient develops between fluid in the subarachnoid space and fluid in the ventricles, which leads to a decrease in CSF production and a higher, yet still normal, CSF pressure. It is this new pressure that begins to distend the ventricles. Ventricular distention stretches surrounding nerve fibers and compresses the periventricular parenchyma. This compression is thought to lead to ischemia by its impinging on arterioles and capillaries (Vanneste, 2000).

Symptoms of NPH

Symptoms of NPH can appear suddenly (when caused by trauma or injury) but usually appear slowly and insidiously over a period of months, or more often, years. Although a triad of symptoms is often described in the literature, all three symptoms are not required for a diagnosis of NPH. The first symptom to appear in most patients is usually evidence of a frontal disequilibrium gait disturbance, followed by cognitive impairment and urinary incontinence (D’Abreau, 2004). Because these symptoms appear slowly and are associated with many disorders of aging, it is easy to understand why NPH goes unrecognized and undiagnosed.

Gait Disturbance

The distinctive gait pattern of NPH consists of slow shuffling, small steps, and an exaggerated wide stance (Krauss et al., 2001). Patients with NPH also exhibit poor posture with a forward rounding and tilting of the shoulders and arms that hang loosely at their sides. They appear to always be watching their feet as they attempt to move. Patients with NPH describe their feet as feeling like they are “stuck to the floor” or “weighted down with cement.” Their feet rarely leave the ground as they shuffle forward, and they appear to have difficulty initiating the first step when ambulating.

Gait apraxia is commonly used to describe the gait associated with NPH. Gait apraxia consists of difficulty sequencing the required movements needed for ambulation (strike, stance, and swing) as well as uncoordinated attempts to alter course or maintain continuous movement (Verrees & Selman, 2004). As a result of gait disturbances, falls are a frequent and potentially life-threatening problem associated with NPH. Left untreated, gait problems continue to progress until total inability to ambulate leaves patients confined to a wheelchair or a bed.

The gait-related symptoms of NPH are in many ways similar to those associated with Parkinson’s disease, which also presents with gradual gait and balance problems and a general slowness of movement (bradykinesia). One difference between Parkinson’s disease and NPH is that patients with Parkinson’s disease usually exhibit fine tremors of the hands coupled with rigidity and stiffness of the limbs and trunk, which is not usually seen in patients with NPH. Instead, patients with NPH display limpness of the extremities.

Cognitive Impairment

The second characteristic feature of NPH is a change in cognitive function and mentation. It is important to note that this symptom is not always present in patients with NPH. When dementia symptoms are present, they are subcortical, rather than cortical, symptoms. Cortical dementias arise from a disorder affecting the cerebral cortex, the outer layer of the brain that plays a critical role in cognitive processes. Alzheimer’s disease and Creutzfeldt-Jakob disease are two forms of cortical dementia. Patients with cortical dementia typically exhibit severe memory impairment and aphasia and an inability to recall words and understand common language. In contrast, subcortical dementias are the result of a dysfunction in the parts of the brain beneath the cortex. The memory loss and language difficulties characteristic of cortical dementias are usually not present. Inattention, latency in recall, and lack of spontaneity are characteristics of subcortical dementia (Cleveland Clinic Health System, 2004).

Thus, the mentation associated with NPH is characterized by a lack of spontaneity in movement (psychomotor slowness), verbal responses, and emotions, as well as slowness processing information, responding to questions, or reacting to situations. When questioned, patients with NPH typically can provide the correct answer and correctly recall facts, but their ability to process the content of the question and formulate their response is slowed. This feature of subcortical dementia is useful in differentiating NPH dementia from that found in Alzheimer’s disease, a cortical dementia. Characteristics of cortical dementia, such as problems with word formation and interpretation of contextual stimuli or an inability to perform a series of tasks sequentially, are not usually seen in patients with NPH (D’Abreau, 2004).

Urinary Incontinence

The third NPH symptom is urinary incontinence associated with urinary urgency. It is posited that periventricular corticospinal tract sacral nerve fiber deformation due to ventricular distention is the primary cause of this symptom (Gleason, Black, & Matsumae, 1993). Although troublesome, this symptom is often not reported, as patients may attribute frequent urination, urinary urgency, and incontinence to use of diuretic medications or prostatic problems, and some may consider this a normal aging problem. In addition, urinary incontinence, although often a feature of NPH, is not always present, especially in the early stages of the disorder.

Differential Diagnosis

Identification of patients with NPH is difficult at best. However, prognosis is affected by delay in diagnosis and treatment, so it is important to carefully examine and sufficiently assess all patients who present with gait problems and to initiate early referrals, even when symptoms are loosely suggestive of NPH (Verrees & Selman, 2004). The symptoms of NPH are difficult to distinguish from those of other neurological conditions encountered in an elderly population. Diagnosis becomes more difficult when patients also present with several comorbid conditions that can impair gait, lead to urinary symptoms, and alter cognitive function (Table 1).

Differential Diagnoses in Normal Pressure Hydrocephalus

Table 1: Differential Diagnoses in Normal Pressure Hydrocephalus

Diagnostic Tests

Physical examination, assessment of cortical and subcortical function, and careful analysis of gait, along with a complete record of previous health, are the most important tools to diagnose NPH. When gait, cognition, or urinary symptoms are identified, radiographic imaging (computerized axial tomography and magnetic resonance imaging) should be performed. Radiographic imaging is helpful for ruling out other possible causes for symptoms, especially potentially life-threatening conditions, such as infections, tumors, structural abnormalities, or subdural hematomas (Verrees & Selman, 2004). Evidence of ventricular dilation without hippocampus tissue loss can indicate NPH.

Diagnostic guidelines for a probable, possible, and unlikely diagnosis of idiopathic NPH have been published (Relkin, Marmarou, Klinge, Bergsneider, & Black, 2005) and are condensed in Table 2. Patients who meet either the probable or possible criteria should be referred to a neurologist or neurosurgeon for further evaluation.

Diagnostic Criteria for a Probable, Possible, and Unlikely Diagnosis of Idiopathic Normal Pressure Hydrocephalus

Table 2: Diagnostic Criteria for a Probable, Possible, and Unlikely Diagnosis of Idiopathic Normal Pressure Hydrocephalus

Treatment of NPH

Once diagnosed, patients are screened to determine whether a shunting procedure is likely to successfully reverse their symptoms. Although conflicting evidence has been reported regarding the effectiveness of shunting procedures for NPH, a retrospective study that examined shunting procedures for NPH from 1993 to 2003 found that NPH could be accurately diagnosed with continuous CSF monitoring and a 3-day trial of controlled (10 mL per hour, 240 mL per day) continuous CSF drainage (McGirt et al., 2005). Response to drainage was defined as an objective improvement in gait, cognition, or bladder control, and patients who responded favorably to CSF drainage were likely to have long-term symptom improvement with a permanent shunt. Researchers also found gait disorder as the prominent symptom, and shorter duration of symptoms were significant predictors of likely post-shunt improvement.

The effectiveness of shunting on dementia symptoms associated with NPH has also been reported. Previous studies had reported inconsistent results; however, Duinkerke, Williams, Rigamonti, and Hillis (2004) found that patients with idiopathic NPH who demonstrated clinical improvement in cognitive function in response to CSF drainage were likely to show significant long-term improvement in verbal memory and psychomotor speed with a shunting procedure.

Shunting Procedure

The most common shunting procedure used for NPH is a ventricular peritoneal shunt. A small hole is made in the skull and the ventricular end of a catheter is placed in the lateral ventricle. A catheter is then tunneled under the skin from the top of the head, behind the ear, and down to the abdominal cavity. The CSF fluid is shunted into the peritoneal cavity for removal. The entire procedure usually takes less than 1 hour, but it is not without risks, such as hemorrhage or stroke.

Shunt systems have two major components: a catheter, the tubing that transports and diverts the CSF from the ventricles to either the abdominal cavity (or right atrium), and a shunt that regulates the pressure or flow of CSF from the ventricles. Shunts usually have a flushing chamber (reservoir) that permits removal of CSF samples and allows for testing of flow to determine shunt functioning. Several kinds of shunts are available. Some are programmable, and others remove a fixed amount of fluid at a steady rate. Most procedures today are done with the programmable shunt, which provides a number of programmable pressure settings that are controlled through an external device. This wide range of pressure settings permits fine adjustments to obtain the best symptom relief. Adjusting shunt pressure takes only a few minutes, is noninvasive, and is done in the health care provider’s office. The newest product available, the self-programming shunt, provides position-independent CSF flow and maintains consistent flow even in the presence of magnetic fields, which can affect programmable shunts.

Potential Problems and Complications of Shunting

As mentioned above, shunting procedures carry significant risk, and most problems associated with shunting occur weeks or months after the procedure. For this reason, patients are carefully screened beforehand to ensure they have a likely chance of significant improvement. Potential complications include infections of the surgical sites or of the CSF (meningitis), bleeding into the brain or ventricles, and seizures. One of the most common problems that can occur after a shunting procedure is obstruction. Obstruction is usually detected when patients’ original NPH symptoms reoccur (Table 3). Obstructions, although common, are usually not serious and are easy to correct.

Symptoms of Shunt Malfunction

Table 3: Symptoms of Shunt Malfunction

The most serious shunt-related complication is a subdural hematoma. This can occur when CSF is removed from the ventricles too quickly, causing the surface of the brain to pull away from the skull. However, a subdural hematoma is usually associated with a fall. Even a mild injury to the head can result in a subdural hematoma for NPH patients with a shunt. Symptoms of a subdural hematoma range from headache to paralysis, and subdural hematomas can also cause death.

Nursing Implications

Neurological assessment is an essential component of nursing care for older adults. A more extensive assessment is indicated for patients who present with any of the triad symptoms of NPH. Assessment should include a complete patient history and a careful evaluation of cognition, gait, and changes in urinary patterns. Asking patients or their families about gradual changes over time in mentation and ambulation will help nurses identify the pattern of NPH. Failure to assess for NPH is a critical factor leading to underdiagnosis and undertreatment of NPH.

After patients receive a shunt, nursing implications should center around patient education and early recognition of symptoms related to shunt complications. Patients should be instructed to inform health care staff about their shunt before undergoing any procedures or tests, and they should be taught to report headaches, changes in vision, loss of coordination, fatigue, or difficulty sleeping, as these may be signs of infection, bleeding, or obstruction.

Summary

NPH is a reversible disorder that can easily be overlooked or mistaken for other neurological disorders associated with aging, such as Parkinson’s disease and Alzheimer’s disease. Diagnosis is complicated by the presence of multiple comorbid conditions that also affect gait, cognition, and urinary problems in older patients. Careful and complete assessment of patients who exhibit any of the triad symptoms using the NPH guidelines and early referrals to a specialist are recommended, even if the symptom profile is incomplete.

Treatment consists of shunting CSF from the ventricles, and several devices are currently available. The success of shunting procedures depends on early diagnosis and treatment; shunting complications can and do occur, and some can be life threatening. However, the most recent evidence demonstrates that shunting can be used to successfully reverse both gait abnormalities and cognitive decline, and this reversal of symptoms improves both quality and quantity of life for individuals with NPH. The Sidebar on page 31 lists several other NPH resources.

Hydrocephalus Association, Adult-onset Normal Pressure Hydrocephalus: An update

http://www.hydroassoc.org/newsletter/update.html

Hyman-Newman institute for Neurology and Neurosurgery, Hydrocephalus: NPH

http://nyneurosurgery.org/hydronph.htm

Life NPH: Hope for People with Normal Pressure Hydrocephalus

http://www.allaboutnph.com/

Medtronic: Hydrocephalus: Normal pressure hydrocephalus

http://www.medtronic.com/hydrocephalus/nph/index.html

National institute of Neurological Disorders and stroke: Normal Pressure Hydrocephalus information Page

http://www.ninds.nih.gov/disorders/normal_pressure_hydrocephalus/normal_pressure_hydrocephalus.htm

References

  • Adams, RD, Fisher, CM, Hakim, S, Ojemann, RG & Sweet, WH1965. Symptomatic occult hydrocephalus with “normal” cerebrospinal fluid pressure: A treatable syndrome. New England Journal of Medicine, 273, 117–126.
  • American Association of Neurological Surgeons. 2005. Adult onset hydrocephalus. Retrieved January 9, 2008, from http://www.neurosurgerytoday.org/what/patient_e/adult.asp
  • Casmiro, M, D’Alessandro, R, Cacciatore, PM, Daidone, R, Calbucci, F & Lugarest, E1989. Risk factors for the syndrome of ventricular enlargement with gait apraxia (idiopathic normal pressure hydrocephalus). Journal of Neurology and Neurosurgical Psychiatry, 52, 847–852.
  • Chicago Institute of Neurology and Neuroresearch. 2007. Normal pressure hydrocephalus (NPH): New guidelines for diagnosis and treatment. Retrieved January 9, 2008, from http://www.cinn.org/cr-articles/CR-nph.html
  • Cleveland Clinic. (n.d.). Patient’s guide to normal pressure hydrocephalus (NPH). Retrieved January 9, 2008, from http://cms.clevelandclinic.org/neuroscience/body.cfm?id=113
  • Cleveland Clinic Health Information Center. 2004. Normal pressure hydrocephalus. Retrieved January 9, 2008, from http://www.clevelandclinic.org/health/health-info/docs/3500/3525.asp?index=11569
  • Cleveland Clinic Health System. 2004. Types of dementia. Retrieved July 16, 2007, from http://www.cchs.net/health/health-info/docs/2300/2340.asp?index=9170
  • D’Abreau, A2004. Normal pressure hydrocephalus. Medicine and Health, 87, 372–374.
  • Duinkerke, A, Williams, MA, Rigamonti, D & Hillis, AE2004. Cognitive recovery in idiopathic normal pressure hydrocephalus after shunt. Cognitive and Behavioral Neurology, 17, 179–184. doi:10.1097/01.wnn.0000124916.16017.6a [CrossRef]
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  • Krauss, JK, Faist, M, Schubert, M, Borremans, JJ, Lucking, CH & Berger, W2001. Evaluation of gait in normal pressure hydrocephalus before and after shunting. Advances in Neurology, 87, 301–310.
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  • National Council on Aging. 2004. NCOA to raise awareness of little known condition often mistaken for Alzheimer’s disease. Retrieved January 9, 2008, from http://www.ncoa.org/content.cfm?sectionID=105&detail=578
  • Relkin, N, Marmarou, A, Klinge, P, Bergsneider, M & Black, P2005. Diagnosing idiopathic normal-pressure hydrocephalus. Neurosurgery, 57Suppl. 3, S4–S16.
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  • Verrees, M & Selman, WR2004. Management of normal pressure hydrocephalus. American Family Physician, 70, 1071–1078.
  • Walchenbach, R, Geiger, E, Thomeer, RTWM & Vanneste, JAL2002. The values of temporary external lumbar CSF drainage in predicting outcome of shunting on normal pressure hydrocephalus. Journal of Neurology, Neurosurgery, and Psychiatry, 72, 503–506.
  • Waxman, SG2003. Anatomy of the brain. In Clinical neuroanatomy (25th ed.). Retrieved January 9, 2008, from McGraw-Hill’s AccessMedicine Web site: http://www.accessmedicine.com/content.aspx?aID=151499

Differential Diagnoses in Normal Pressure Hydrocephalus

Symptoms Diagnosis
Cognition or mentation symptoms • Alzheimer’s disease
• Vascular dementia
• Chronic alcoholism
• Brain or spinal cord infection
• Brain tumor
• Hypothyroidism
Gait symptoms • Parkinson’s disease
• Joint disorders
Urinary symptoms • Prostate disorders
• Diuretic medication use

Diagnostic Criteria for a Probable, Possible, and Unlikely Diagnosis of Idiopathic Normal Pressure Hydrocephalus

Assessment Criteria Probable Possible Unlikely
History Slow, insidious, and progressive onset of any one of the triad symptoms: X
  • Gait disturbances X X
  • Change in cognition and mentation X X
  • Urinary frequency or incontinence X X
Undetermined onset or progression of any one of the triad symptoms X
Sudden onset of any one of the triad symptoms X
Imaging Ventricular enlargement or dilation X X
No ventricular enlargement or dilation X
Mentation Subcortical symptoms: X X
  • Slowness processing information X X
  • Slowness responding to questions X X
  • Slowness responding to situations X X
  • Decreased fine motor speed or accuracy X X
Cortical symptoms: X
  • Memory loss X
  • Language difficulties X
Gait Decreased height and length of steps X X
Wide stance X X
Swaying X X
Impaired balance X X
Difficulty getting out of a chair X X
En bloc turning X X
Urinary symptoms Frequent urination not explained by other conditions or use of diuretic medications X X
Persistent urinary incontinence X X
Nocturnal incontinence X X

Symptoms of Shunt Malfunction

• Difficulty waking up or staying awake
• Headache
• Incontinence
• Irritability
• Loss of coordination or balance
• Mild dementia
• Personality change
• Return of gait disturbance
• Tiredness
• Vision problems

Hydrocephalus Association, Adult-onset Normal Pressure Hydrocephalus: An update

http://www.hydroassoc.org/newsletter/update.html

Hyman-Newman institute for Neurology and Neurosurgery, Hydrocephalus: NPH

http://nyneurosurgery.org/hydronph.htm

Life NPH: Hope for People with Normal Pressure Hydrocephalus

http://www.allaboutnph.com/

Medtronic: Hydrocephalus: Normal pressure hydrocephalus

http://www.medtronic.com/hydrocephalus/nph/index.html

National institute of Neurological Disorders and stroke: Normal Pressure Hydrocephalus information Page

http://www.ninds.nih.gov/disorders/normal_pressure_hydrocephalus/normal_pressure_hydrocephalus.htm

Normal-Pressure Hydrocephalus

Siedlecki, SL2008. Normal Pressure Hydrocephalus: Are You Missing the Signs?Journal of Gerontological Nursing, 342, 27–33.

  1. The triad of symptoms of normal pressure hydrocephalus (NPH) includes gait disturbances, changes in cognition, and urinary frequency or incontinence.

  2. Gait disturbances are the most prominent and often earliest symptom associated with NPH.

  3. Symptoms of NPH mimic other disorders common among older adults, making it difficult to diagnose.

  4. NPH is a reversible condition if diagnosed and treated early.

Authors

Dr. Siedlecki is Senior Nurse Researcher, Cleveland Clinic, Cleveland, Ohio.

The author discloses that she has no significant financial interests in any product or class of products discussed directly or indirectly in this activity, including research support.

Address correspondence to Sandra L. Siedlecki, PhD, RN, CNS, Senior Nurse Researcher, Cleveland Clinic, 9500 Euclid Avenue P32, Cleveland, OH 44195; e-mail: .siedles@ccf.org

10.3928/00989134-20080201-11

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